Chapter 14
potassium leads to an increased extracellular potassium con-
centration, which in turn directly stimulates the adrenal cor-
tex to produce aldosterone. The increased plasma aldosterone
concentration increases potassium secretion and thereby elimi-
nates the excess potassium from the body.
Conversely, a lowered extracellular potassium concen-
tration decreases aldosterone production and thereby reduces
potassium secretion. Less potassium than usual is excreted in
the urine, thereby helping to restore the normal extracellular
Figure 14–30
summarizes the control and major renal
tubular effects of aldosterone. The fact that a single hormone
regulates both sodium and potassium excretion raises the
question of potential confl icts between homeostasis of the two
ions. For example, if a person was sodium-defi cient and there-
fore secreting large amounts of aldosterone, the potassium-
secreting effects of this hormone would tend to cause some
potassium loss even though potassium balance was normal to
start with. Usually, such confl icts cause only minor imbalances
because there are a variety of other counteracting controls of
sodium and potassium excretion.
Renal Regulation of Calcium
and Phosphate
Calcium and phosphate balance are controlled primarily by
parathyroid hormone and 1,25(OH)
D, as described in detail
in Chapter 11. Approximately 60 percent of plasma calcium
is available for fi ltration in the kidney. The remaining plasma
calcium is protein-bound or complexed with anions. Because
calcium is so important in the function of virtually every cell
in the body, the kidney has powerful mechanisms to reabsorb
calcium from the tubular fl
uid. More than 60 percent of cal-
cium reabsorption is not under hormonal control and occurs
in the proximal tubule. The hormonal control of calcium reab-
sorption occurs mainly in the distal convoluted tubule and
early in the cortical collecting duct. When plasma calcium is
low, the secretion of parathyroid hormone (PTH) from the
parathyroid glands increases. PTH stimulates the opening of
calcium channels in these parts of the nephron, thereby increas-
ing calcium reabsorption. As discussed in Chapter 11, another
important action of PTH in the kidney is to increase the activ-
ity of the 1-hydroxylase enzyme, thus activating 25(OH)-D to
D, which then goes on to increase calcium and
phosphate absorption in the gastrointestinal tract.
About half of the plasma phosphate is ionized and is fi l-
terable. Like calcium, most of the phosphate that is fi
is reabsorbed in the proximal tubule. Unlike calcium, phos-
phate reabsorption is decreased by PTH, thereby increasing
the excretion of phosphate. Thus, when plasma calcium is low,
and PTH and calcium reabsorption are increased as a result,
phosphate excretion is increased.
Summary—Division of Labor
Table 14–5
summarizes the division of labor of renal func-
tion along the renal tubule. So far, we have discussed all of
these processes except the transport of acids and bases, which
Section C of this chapter will cover.
Cortical collecting ducts
Plasma aldosterone
Adrenal cortex
Aldosterone secretion
Plasma angiotensin
Plasma volume
Plasma potassium
(As in Fig. 14–22)
Figure 14–30
Summary of the control of aldosterone and its effects on sodium
reabsorption and potassium secretion.
Figure 14–29
Pathways by which an increased potassium intake induces greater
potassium excretion.
Potassium excretion
Cortical collecting ducts
Potassium secretion
Plasma aldosterone
Adrenal cortex
Aldosterone secretion
Plasma potassium
Potassium intake
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